Causes, symptoms and treatment of trigeminal neuralgia. Trigeminal neuralgia. Causes, symptoms, signs, diagnosis and treatment of pathology Trigeminal neuralgia treatment

MATERIAL FROM THE ARCHIVE

INTRODUCTION. In the International Classification of Diseases, 10th revision (ICD-10), “trigeminal nerve lesions” include “trigeminal neuralgia (syndrome, pain tic)”, “atypical facial pain”, as well as “other trigeminal nerve lesions” and “trigeminal nerve lesions”. nerves, unspecified."

The International Headache Society (IHS), in the section “Cranial neuralgia, pain due to damage to nerve trunks and deafferentation pain”, considers trigeminal neuralgia as “idiopathic” and “symptomatic” (“with compression of the trigeminal root or ganglion” and with “central lesions”), and also as “facial pain not included in this group.”

In the classification proposed by the International Association for the Study of Pain (IABP), in the section “Neuralgia of the head and face” there are “trigeminal neuralgia (painful tic)”, “secondary trigeminal neuralgia with damage to the central nervous system”, “secondary trigeminal neuralgia with facial trauma” , “acute herpetic and postherpetic trigeminal nerve”, “SUNCT-syndrome” (English abbreviation: short-term, one-sided, neuralgia-like pain with conjunctivitis and lacrimation), “Reder syndrome”, “cluster tic” syndrome.

According to the accepted classification, primary (idiopathic, essential) and secondary (symptomatic) trigeminal neuralgia are distinguished. The first includes trigeminal neuralgia, which develops regardless of any previously occurring pathological process, the second includes symptom complexes that are a complication of the primary disease (viral infection, multiple sclerosis, tumors of the cerebellopontine angle, etc.). However, given the fact that a detailed examination in the vast majority of “idiopathic” trigeminal neuralgia reveals vascular* compression of the trigeminal root, we can conclude that “secondary” forms of the disease predominate.

*In accordance with the modern concept of the etiopathogenesis of trigeminal neuralgia, the leading place in its etiology is occupied by vascular compression of the trigeminal nerve root by an abnormal loop of an artery or vein. This etiological factor was first identified in the work of P. Jannetta in 1967. Vascular compression is detected in 80-90% of cases of all trigeminal neuralgia. The most typical localization of compression is in the proximal part of the trigeminal root within a few millimeters from the entrance of the root into the pons (the so-called root entry zone). In approximately 80% of cases, compression occurs by an arterial vessel, in 20% by a venous vessel, and the latter variant of neurovascular conflict is prognostically the least favorable. Much less commonly, compression is caused by aneurysms of the cerebellopontine angle or arteriovenous malformations. There are other etiological factors for compression of the trigeminal root (tumors localized in the posterior or middle cranial fossa, basal meningitis, etc.).

There are also typical and atypical trigeminal neuralgia...

ATYPICAL TRIGEMINAL NEURALGIA. There are also typical and atypical trigeminal neuralgia. With typical trigeminal neuralgia, the patient does not have any symptoms in the state between paroxysms. With atypical trigeminal neuralgia (trigeminal neuralgia with a predominance of the peripheral component), a “background” aching or burning pain is noted in the interictal interval. It is noted that an atypical variant of trigeminal neuralgia may appear as a result of progression of the “classical” form of neuralgia. The development of one or another form of trigeminal neuralgia is determined by the level of damage to the trigeminal system.

In accordance with topographic and anatomical features, several nosological forms are differentiated: (1) trigeminal neuropathy, (2) trigeminal ganglioneuropathy, (3) deafferentation trigeminal prosopalgia (atypical forms of trigeminal neuralgia) and (4) trigeminal neuralgia proper (typical), when the lesion is localized at the level of the trigeminal root.

However, with a topographic-anatomical approach, one should take into account the fact that a lesion at one level can lead to pathological changes in other trigeminal structures (for example, compression at the level of a root or nerve can, due to disruption of axonal flow, lead to pathological changes in the sensory neurons of the trigeminal ganglion). Therefore, in some cases it is not possible to establish at what level the damage to the trigeminal system began.

Atypical trigeminal neuralgia is characterized by a wave-like course with alternating periods of increased pain and remissions. Many patients often show signs of depression. Trigeminal neuropathy must be ruled out before diagnosing atypical trigeminal neuralgia. Trigeminal neuropathy, in contrast to neuralgia, is manifested mainly by symptoms of prolapse: decreased sensitivity in the areas of innervation of the branches of the trigeminal nerve, decreased taste sensitivity, atrophy and weakness of the masticatory muscles.

In the clinic of trigeminal neuropathies of predominantly peripheral origin, in contrast to “typical” trigeminal neuralgia, there are a number of features: (1) pain initially occurs at the site of localization of the primary pathological process (tumors, foci of inflammation, trauma, etc.); (2) paroxysmal pain is often preceded by prolonged and painful pain in the area of ​​innervation of the corresponding branch of the trigeminal nerve; (3) the pain syndrome, intensifying in attacks, lasts for a long time (hours and days), weakening gradually; (4) painful manifestations may be limited to the branching zone of individual nerves within the main branches of the trigeminal nerve, dental plexuses or their branches, etc.; (5) novocaine and alcohol novocaine blockades lead to a very short-term improvement, giving a therapeutic effect only for the period of action of novocaine; in the future, as a rule, an increase in pain occurs; (6) a noticeable therapeutic effect is achieved by taking analgesics; (7) drugs of the carbamazepine group usually either cause very little pain relief or are completely ineffective; (8) the clinical picture of neuralgia may vary depending on the state of the underlying pathological process; (9) elimination of the cause of trigeminal syndrome often does not lead to the elimination of neuralgia.

Among trigeminal neuralgia with a predominance of the peripheral component of pathogenesis, the main forms are: (1) odontogenic neuralgia of the trigeminal nerve, (2) dental plexalgia, (3) postherpetic neuralgia, (4) neuralgia with damage to the semilunar ganglion, (5) neuralgia of individual nerves of the main branches trigeminal nerve.

Odontogenic neuralgia of the trigeminal nerve. The main etiological factors that lead to the development of odontogenic neuralgia are pathological processes of the dental system and ineffective or incorrect methods of their treatment. The most common reasons are: (1) traumatic (complex) tooth extractions, including the presence of bone fragments and root remains in the socket; (2) pulpitis and periodontitis; (3) the phenomenon of galvanism when using different metals for fillings and prostheses; (4) poorly made dentures that injure the oral mucosa or violate the height of the bite; (5) gingivitis and other periodontal diseases; (6) osteomyelitis of the jaw bones and other diseases; (7) gingivitis and other periodontal diseases. A combination of the above factors may occur. The clinical picture of the disease is dominated by persistent pain with severe pain syndrome and autonomic disorders. The pain, as a rule, is localized in the area of ​​the pathological focus, intensifying in paroxysms, lasting from several hours to several days, gradually decreasing in intensity. A distinctive feature of odontogenic neuralgia is its long course, despite the elimination of the etiological factor of the disease.

Dental plexalgia . The upper dental plexus is affected more often, the lower - less often (ratio 2:1), which is apparently due to the absence of the latter in 50% of people. Combined lesions are also possible. Most often, odontogenic factors with predominant damage to the terminal branches of the plexus lead to the development of plexalgia. This is possible when it is difficult to remove premolars, molars and wisdom teeth, conduction anesthesia, surgical interventions on the jaws, removing filling material beyond the tops of the root canals, removing a large number of teeth within a short period of time in preparation for oral prosthetics, as well as in case of infectious lesions due to osteomyelitis of the sockets, etc. Injuries, hypothermia, intoxication can be provoking factors. Features of clinical manifestations: dental plexalgia is characterized by constant dull excruciating pain, sometimes intensifying, localized in the innervation zone of the dental plexus on the affected side with repercussion to the healthy side. The dominant focus of pain in dental plexalgia is localized in the area of ​​the alveolar process, gums and teeth. The pain is excruciating, persistent, constant, burning. When the dental plexus is damaged, constant local burning pains sometimes intensify in paroxysms and their intensity increases. Even removing the affected teeth does not relieve the pain, and in some patients it occurs in neighboring teeth. In some patients, the pain decreases during meals, but under the influence of unfavorable meteorological factors or emotions it intensifies. The attack, as a rule, begins with a mild dull pain; after 20-30 minutes, at the height of the paroxysm, it acquires a pronounced sympathalgic character, and vasomotor disorders occur. When the attack is stopped, a dull pain remains in the alveolar process of the jaw. When the upper dental plexus is damaged, pain can radiate along the second branch of the trigeminal nerve and be accompanied by severe autonomic disorders. When examining patients with dental plexalgia, severe pain is detected in the area of ​​​​the projection of the affected dental plexus. On palpation, pain is noted in the projection of the dental plexus (when pressing both on the mucous membrane of the gums and in the area of ​​the facial skin). A significant number of patients experience hyperesthesia of the mucous membrane of the gums and the mucous membrane of the inner surface of the cheek and teeth in the area of ​​the affected dental plexus. As a rule, patients with dental plexalgia experience a decrease in pain when eating rough food and an increase in pain under the influence of emotions, hypothermia, and unfavorable meteorological factors. When the upper dental plexus is damaged, during painful paroxysm, pain can radiate to the hard palate, zygomatic, cheek, infraorbital region, temple, ear, occipital region, and involve the entire half of the head and the upper third of the neck. When the lower dental plexus is damaged, the pain spreads to the floor of the mouth, buccal, parotid-masticatory areas, and upper neck. The attacks are accompanied by a variety of autonomic symptoms, which are caused by connections of the plexus with the autonomic ganglia (pterygopalatine ganglion and superior cervical sympathetic ganglion). When differential diagnosis with trigeminal neuralgia, important signs of dental plexalgia can be: (1) absence of trigger zones; (2) absence of pain during palpation at the points where the trigeminal nerve exits the face; (3) the presence of pain on palpation of the dental plexus area; (4) attacks of pain with dental plexalgia are longer in nature (up to 20 minutes or more); (5) with dental plexalgia in the interictal period, localized pain remains in the alveolar process in the projection of the dental plexus; (6) the irradiation of pain often does not correspond to the anatomical location of the branches of the trigeminal nerve.

Postherpetic trigeminal neuralgia. Herpes zoster is an infectious disease caused by a neurotropic filterable virus. This virus is close or identical to the chickenpox virus. It has now been established that when suffering from herpes, various parts of the nervous system are affected, mainly the ganglia and sensory roots, as well as the membranes of the brain, where infiltration phenomena with hemorrhagic foci are observed. When the nervous system is damaged by the herpes zoster virus, the following forms of pain syndromes in the facial area are possible: (1) headaches and facial pain of a diffuse nature, which is one of the manifestations of the meningeal symptom complex; (2) acute trigeminal neuralgia; (3) early postherpetic neuralgia (lasting up to 6 months); (4) late postherpetic neuralgia (lasting from 6 months to several years).

PRINCIPLES OF TREATMENT OF ATYPICAL TRIGEMINAL NEURALGIA. Non-narcotic analgesics (analgin, efferalgai, baralgin, tramadol) intramuscularly and intravenously are indicated. At the same time, non-steroidal anti-inflammatory drugs are prescribed: (1) salicylates (acetylsalicylic acid - 0.25 - 0.5 g 3 - 4 times a day after meals, quversalin - 1 - 3 tablets 3 - 4 times a day, which can be taken and before meals, etc.); (2) pyrazolone derivatives (butadione 0.2 g 3 times a day, reopirin, pyrabutol, tribuzone - 0.25 g 3-4 times a day after meals); (3) derivatives of indoleacetic, phenylacetic, phenylpropionic and anthrapylic acids (indomethacin - 25 mg 2 - 3 times a day, bringing the daily dose to 100-150 mg, can be combined with salicylates; ibuprofen - 0.2 - 0.4 g 3 once a day; diclofenac sodium, diclofenac potassium, naproxen, mefenamic acid, chlotazol); (4) para-aminophenol derivatives (efferalgan - 0.5 g 2 - 3 times a day, sedalgin - 1 tablet 3 times a day).

Use the non-steroidal anti-inflammatory drug ketorolac (ketorol) 1 ml intramuscularly or 10 mg orally 3 times a day. It has a pronounced analgesic effect. Prodeine is effective. Analgesics are used in combination with antihistamines (fenkarol, diphenhydramine, diprazine, suprastin, diazolin, tavegil), as well as with tranquilizers and neuroleptics (aminazine, thioridazine, haloperidol).

It is advisable to prescribe drugs with an antidepressant effect in combination with the listed drugs (amitriptyline - 0.025 g 2-3 times a day, as well as selective serotonin reuptake inhibitors: fluvoxamine, paroxetine, sertraline, etc.). In case of significantly severe pain syndrome, neuroleptanalgesia is indicated as a one-time emergency measure - intramuscular injection of 2 - 3 ml of 0.25% solution of droperidol in combination with the synthetic analgesic fentanyl (2 ml of 0.005% solution).

For persistent pain that is difficult to treat, use a mixture of the following composition: 2 ml of a 50% analgin solution, 1 ml of a 2% promedol solution, 2 ml of a 0.5% novocaine solution.

Vitamins of group B (B1, B12 and their analogs) are indicated, as well as physiotherapy: dynamic or sinusoidal currents, ultrasound, moderate heat, electrophoresis of novocaine or calcium chloride, phonophoresis of hydrocortisone with analgin. In the future, mud therapy, paraffin, ozokerite, biostimulants, aloe, and acupuncture are recommended. Be sure to sanitize the oral cavity.

For dental plexalgia, non-narcotic analgesics are prescribed in combination with tranquilizers and neuroleptics, anesthetic or lidocaine ointment on the gums, B vitamins, and atropine group alkaloids. Specialized care includes a dental examination of the patient, preferably carried out in a multidisciplinary dental clinic using radiography, electro-odontodiagnosis, etc. If pathology of the pulp, marginal or apical periodontium, inflammatory diseases of the maxillofacial area, incorrectly manufactured dentures, as well as neoplasms are detected, appropriate treatment is carried out.

In the treatment of odontogenic neuralgia, a good therapeutic effect is achieved by taking analgesics. Drugs of the carbamazepine group sometimes provide a slight reduction in pain, but are often ineffective. To treat pain syndrome with odontogenic neuralgia, a combination of analgesics, antihistamines, and antidepressants is prescribed in combination with measures aimed at eliminating the pathological focus that caused the development of the disease. Acupuncture and physiotherapy (diadynamic or sinusoidal modulated currents, ultrasound, UHF therapy) have a certain effect. During the recovery period, mud therapy, ozokerite or paraffin therapy are carried out, biogenic stimulants are used in a course of 10 - 15 injections.

Trigeminal neuralgia (Trousseau's pain tic, Fothergill's disease, trigeminal neuralgia) is a fairly common disease of the peripheral nervous system, the main symptom of which is paroxysmal, very intense pain in the area of ​​innervation (connection with the central nervous system) of one of the branches of the trigeminal nerve. The trigeminal nerve is a mixed nerve; it provides sensory innervation to the face and motor innervation to the masticatory muscles.

A wide variety of factors underlying the disease, excruciating pain, social and work maladjustment, long-term drug treatment with delayed treatment are not the entire range of reasons that keep this problem at the top of the ranking of neurological diseases. The symptoms of trigeminal neuralgia are quite easily recognizable even by non-professionals, but only a specialist can prescribe treatment. We will talk about this disease in this article.

Causes of trigeminal neuralgia

The trigeminal nerve is the 5th pair of cranial nerves. A person has two trigeminal nerves: left and right; The disease is based on damage to its branches. In total, the trigeminal nerve has 3 main branches: the ophthalmic nerve, the maxillary nerve, the mandibular nerve, each of which breaks up into smaller branches. All of them, on their way to the innervated structures, pass through certain openings and channels in the bones of the skull, where they can be subject to compression or irritation. The main reasons for this can be systematized as follows:

• congenital narrowing of the holes and canals along the branches;
• pathological changes in the vessels located next to the nerve (aneurysms, or protrusions of arterial walls, any abnormalities in vascular development, atherosclerosis) or their abnormal location (usually the superior cerebellar artery);
• cystic-adhesive processes in the area of ​​branches of the trigeminal nerve as a result of ocular, otorhinolaryngological, dental diseases (inflammation of the sinuses - frontal sinusitis, sinusitis, ethmoiditis; odontogenic periostitis, pulpitis, caries, iridocyclitis, etc.);
• metabolic disorders (diabetes mellitus, gout);
• chronic infectious diseases (tuberculosis, brucellosis, syphilis, herpes);
• tumors (any, localized along the nerve);
• hypothermia of the face (draft);
• facial and skull injuries;
• rarely - brainstem stroke.

The pathological process can affect both the entire nerve and its individual branches. More often, of course, damage to one branch occurs, but in most cases, untimely treatment leads to progression of the disease and involvement of the entire nerve in the pathological process. There are several stages during the course of the disease. At a late stage (third stage of the disease), the clinical picture changes and the prognosis for recovery significantly worsens. Establishing the cause of the disease in each specific case allows you to most effectively select treatment and, accordingly, speed up healing.

Symptoms

The disease is more typical for middle-aged people, most often diagnosed at 40-50 years of age. Females suffer more often than males. Damage to the right trigeminal nerve is most often observed (70% of all cases of the disease). Very rarely, trigeminal neuralgia can be bilateral. The disease is cyclical, that is, periods of exacerbation are followed by periods of remission. Exacerbations are more typical in the autumn-spring period. All manifestations of the disease can be divided into several groups: pain syndrome, motor and reflex disorders, vegetative-trophic symptoms.

Pain syndrome

Nature of the pain: the pain is paroxysmal and very intense, excruciating, sharp, burning. During an attack, patients often freeze and do not even move; they compare the pain to the passage of an electric current, or a shooting sensation. The duration of the paroxysm is from several seconds to several minutes, but during the day the attacks can be repeated up to 300 (!) times.

Localization of pain: pain can affect both the innervation zone of one of the branches and the entire nerve on one side (right or left). One of the features of the disease is the irradiation (spread) of pain from one branch to another, involving the entire half of the face. The longer the disease exists, the more likely it is to spread to other branches. Localization zones:

• optic nerve: forehead, anterior scalp, bridge of the nose, upper eyelid, eyeball, inner corner of the eye, mucous membrane of the upper part of the nasal cavity, frontal and ethmoid sinuses;
• maxillary nerve: upper part of the cheek, lower eyelid, outer corner of the eye, upper jaw and its teeth, wing of the nose, upper lip, maxillary sinus, mucous membrane of the nasal cavity;
• mandibular nerve: lower part of the cheek, chin, lower jaw and its teeth, lower surface of the tongue, lower lip, mucous membranes of the cheeks. The pain can radiate to the temple, back of the head, neck. Sometimes the pain is clearly localized in the area of ​​one tooth, which prompts patients to go to the dentist. However, treating this tooth does not eliminate the pain.

Pain provocation: the development of pain paroxysm can be caused by touching or light pressure on the so-called trigger (trigger) zones. These zones are quite variable in each individual patient. Most often this is the inner corner of the eye, the back of the nose, the eyebrow, the nasolabial fold, the wing of the nose, the chin, the corner of the mouth, the mucous membrane of the cheek or gum. An attack can also be provoked by pressing on the exit points of the branches on the face: the supraorbital, infraorbital, and mental foramen. Pain can also be caused by talking, chewing, laughing, washing your face, shaving, brushing your teeth, applying makeup, even blowing wind.

Behavior during an attack: patients do not cry, do not scream, but freeze, trying not to move, rubbing the pain area.

Motor and reflex disorders:

• spasms of the facial muscles (hence the name of the disease “painful tic”): during a painful attack, involuntary muscle contraction develops in the orbicularis oculi muscle (blepharospasm), in the masticatory muscles (trismus), and in other facial muscles. Often muscle contractions extend to the entire half of the face;
• changes in reflexes - superciliary, corneal, mandibular - which is determined during a neurological examination.

Vegetative-trophic symptoms: observed at the time of the attack, in the initial stages they are slightly expressed, and as the disease progresses, they are necessarily accompanied by a painful paroxysm:

• skin color: local pallor or redness;
• changes in gland secretion: lacrimation, drooling, runny nose;
• late signs: develop with long-term existence of the disease. There may be swelling of the face, greasy or dry skin, and loss of eyelashes.

In the late stage of the disease, a focus of pathological pain activity forms in the visual thalamus (thalamus) in the brain. This leads to a change in the nature and location of pain. Eliminating the cause of the disease in this case no longer leads to recovery. The distinctive features of this stage of the disease are as follows:

• pain spreads to the entire half of the face from the onset of paroxysm;
• touching any part of the face causes pain;
• Even the memory of it can lead to a painful paroxysm;
• pain may occur in response to stimuli such as bright light or loud sound;
• the pain gradually loses its paroxysmal nature and becomes constant;
• vegetative-trophic disorders intensify.

Diagnostics

The main role in establishing a diagnosis belongs to carefully collected complaints and anamnesis of the disease. During a neurological examination, it is possible to identify areas of decreased or increased sensitivity on the face, as well as changes in the following reflexes:

• superciliary - that is, closing the eyes while tapping along the inner edge of the superciliary arch;
• corneal - that is, the effect of closing the eyes in response to external stimuli;
• mandibular - that is, contraction of the masticatory and temporal muscles during tapping on the lower jaw).

During the period of remission, a neurological examination may not reveal any pathology. To find the cause of neuralgia, the patient may be shown magnetic resonance imaging (MRI), but it does not always reveal the truth.

Treatment

The main methods of treating trigeminal neuralgia include:

• medicinal;
• physiotherapy;
• surgical treatment.

The main drug used in drug treatment remains carbamazepine (Tegretol). It has been used in the treatment of this disease since 1962. It is used according to a special scheme: the initial dose is 200-400 mg/day,
gradually the dose is increased and brought to 1000-1200 mg/day in several doses. Once the clinical effect is achieved (cessation of painful attacks), the drug in a maintenance dose is used for a long time to prevent the occurrence of attacks, then the dose is also gradually reduced. Sometimes the patient has to take the drug for 6 months or more. Currently, oxcarbazepine (Trileptal) is also used, which has the same mechanism of action as carbamazepine, but is better tolerated.

In addition to carbamazepine, baclofen 5-10 mg 3 times a day (the drug should also be discontinued gradually) and amitriptyline 25-100 mg/day are used to relieve pain. Of the new drugs synthesized in recent decades, gabapentin (gabagamma, tebantin) is used. When treating with gabapentin, it is also necessary to titrate the dose until it is clinically effective (the initial dose is usually 300 mg 3 times a day, and the effective dose is 900-3600 mg/day), followed by a stepwise reduction until the drug is discontinued. In order to relieve severe exacerbations, sodium hydroxybutyrate or diazepam can be used intravenously. Complex therapy uses nicotinic acid, trental, cavinton, phenibut, pantogam, glycine, B vitamins (milgamma, neurorubin).

Physiotherapeutic treatment is quite varied. Diadynamic currents, electrophoresis with novocaine, ultraphonophoresis with hydrocortisone, acupuncture, and laser therapy can be used. Physiotherapeutic techniques are used only in combination with drug treatment to achieve a faster and better effect.

In the absence of effect from conservative treatment, as well as in cases where trigeminal neuralgia is caused by compression of the root by an anatomical formation, surgical treatment methods are used:

• if the cause of compression is a pathologically altered vessel, then microvascular decompression is performed. The essence of the operation is to separate the vessel and the nerve using microsurgical techniques. This operation is highly effective, but very traumatic;
• percutaneous stereotactic rhizotomy: the nerve root is destroyed using an electric current supplied to the nerve using a needle in the form of an electrode;
• percutaneous balloon compression: stopping pain impulses along a nerve by compressing its fibers using a balloon brought to the nerve using a catheter;
• glycerin injections: destruction of the nerve using glycerin injections into the nerve branch sites;
• nerve destruction using ionizing radiation: non-invasive technique using radiation;
• radiofrequency ablation: destruction of nerve fibers using high temperature;
• If the cause is a tumor process, then, of course, removal of the tumor comes to the fore.

A characteristic feature of all surgical methods is a more pronounced effect when performed early. Those. The earlier this or that operation is performed, the higher the likelihood of cure. It should also be borne in mind that the disappearance of pain attacks does not occur immediately after surgical treatment, but somewhat remotely (the timing depends on the duration of the disease, the extent of the process and the type of surgical intervention). Therefore, all patients with trigeminal neuralgia need timely consultation with a doctor. Previously, the technique of injecting ethyl alcohol into the nerve branching sites was used. Such treatment often gave a temporary effect and had a high incidence of complications. As the nerve regenerated, the pain returned, so today this method of treatment is practically not used.

Prevention

Of course, it is not possible to influence all probable causes of the disease (for example, congenital narrowness of the canals cannot be changed). However, many factors in the development of this disease can be prevented:

• avoid hypothermia of the face;
• promptly treat diseases that can cause trigeminal neuralgia (diabetes mellitus, atherosclerosis, caries, sinusitis, frontal sinusitis, herpetic infection, tuberculosis, etc.);
• prevention of head injuries.

It should also be taken into account that methods of secondary prevention (i.e. when the disease has already manifested itself once) include high-quality, complete and timely treatment.

Video version of the article:

TVC channel, “Doctors” program on the topic “Trigeminal neuralgia”

For quotation: Manvelov L.S., Tyurnikov V.M., Kadykov A.V. Trigeminal neuralgia: epidemiology, etiology, pathomorphology, pathogenesis, clinical picture, diagnosis // Breast cancer. 2013. No. 10. P. 542

Trigeminal neuralgia, or trigeminal neuralgia (TN), is the most severe and common form of facial pain. The disease has been known since ancient times, but it was first described by M. Andre only in 1756. The author cited 5 cases of suffering, which he called “painful tic.” A detailed description of TN was presented by J. Fothergil in the monograph “Painful lesions of the face,” which is deservedly considered a fundamental guide. Currently, in the context of the rapid progress of science, the study of the complex problem of TN involves a multidisciplinary approach using epidemiological, clinical, pathomorphological, neuroimaging, ultrasound, electrophysiological, biochemical, pharmacological and other modern research methods; development and implementation of new methods of conservative and surgical treatment into practical healthcare.

There are primary (idiopathic, essential) and secondary (symptomatic) TN. The first includes TN, which occurs regardless of any disease or existing pathological process. In the vast majority of cases of idiopathic TN, vascular compression of the trigeminal root is detected. The second form of TN is a complication of a particular disease: viral or bacterial infection, multiple sclerosis, tumors of the cerebellar pontine angle. In terms of prevalence, the secondary form of TN predominates.
Epidemiology
According to the World Health Organization, the prevalence of TN in various countries is 2-5 people per 100 thousand population per year. Women get sick more often than men (in a ratio of 3:2). The disease can begin at any age, even childhood, but in 80-90% of cases it debuts over the age of 40 years. Moreover, the idiopathic form of TN is most often observed in older people, and the symptomatic form (for example, with multiple sclerosis, tumors, vascular malformations) - in young people.
Etiology
A large number of studies have been devoted to the study of the etiology of TN, especially in recent years. A connection has been proven between paroxysms of pain and compression of the trigeminal nerve root. An important role in the occurrence of TN is played by vascular formations (loops, arteriovenous malformations, aneurysms), as well as multiple sclerosis, tumors and cysts of the cerebellar-pontine angle. According to one hypothesis, TN is a variant of neuropathy.
Until now, the question of the leading role of central or peripheral mechanisms in the etiology and pathogenesis of trigeminal paroxysms remains debatable.
After the introduction of anticonvulsants into practice, there was an assumption about epileptiform activity in the brainstem trigeminal structures as the main cause of paroxysms of pain. However, according to modern concepts, the leading cause of TN is vascular compression of the trigeminal root. In 1967, this reason was first named by P. Jannetta. Vascular compression of the trigeminal root is detected in 80-90% of cases of TN. Most often, compression occurs in the proximal part of the trigeminal root at its entrance to the pons. In 80% of cases, the root is compressed by an artery and in 20% by a vein. The latter is considered the most unfavorable for the prognosis. Less commonly, compression is caused by aneurysms of the cerebellopontine angle and arteriovenous malformations.
Compression of the trigeminal nerve root can also be caused by tumors in the middle and posterior cranial fossae, basal meningitis, vestibular schwannomas, meningiomas, epidermoid cysts and other space-occupying formations. Dysplasia of the structures of the posterior cranial fossa plays a certain role in the development of TN.
Family forms of TN
A number of works have described familial forms of TN. The genetic defect is localized on chromosome 32P. Hereditary syndromes considered risk factors for TN include autosomal dominant hypertension and brachydactyly. Hereditary hypertension is often associated with vascular abnormalities: pathological tortuosity or stenosis of the posterior inferior cerebellar or vertebral arteries. As a result, TN develops due to compression of the ventrolateral parts of the medulla oblongata.
Pathomorphology
In 1994, D. Hilton et al. first described ultrastructural changes in the trigeminal nerve root during vascular compression. The authors found localized axonal demyelination. An immunohistological study revealed that astrocyte processes were localized predominantly at the periphery of the damage. Later, near the demyelinated axons of the damaged trigeminal root, electron microscopy revealed changes in the extracellular space and a large number of collagen fibrils. Increased collagen synthesis and the formation of large aggregates were noted in the central region of the trigeminal nerve root damaged by axonopathy.
Pathogenesis
The primary pathogenetic factor in the occurrence of trigeminal pain is considered to be long-term vascular compression of the trigeminal nerve, which leads to its damage and local demyelination of sensory axons. As a result, a complex of pathophysiological and pathobiochemical disorders is formed, leading to the occurrence of paroxysms of pain. This concept is confirmed by neuroimaging data (detection of microvascular compression of the trigeminal root) and the results of many thousands of microvascular decompression operations, which provide stable and long-term remission of neuralgic syndrome. In addition, the results of experimental work show that decompression promotes remyelination of the trigeminal root and normalization of excitation.
However, for a neurovascular conflict to occur, the following conditions are necessary:
1. dolichoectasia of the superior cerebellar artery;
2. special location of the loop of the superior cerebellar artery;
3. vascular atherosclerosis, leading to a decrease in the elasticity of blood vessels and an increase in the mechanical effect of the pulse wave on the trigeminal nerve root.
In addition, it is known that compression of the branches of the trigeminal nerve in the bone canals of the facial skull can be an etiological factor. These mechanical stresses cause local demyelination of trigeminal neurons, similar to multiple sclerosis, which is the most common cause of secondary TN.
Local demyelination is important in the pathogenesis of TN, causing ephaptic transmission between damaged and undamaged fibers, forming a generator of pathologically enhanced excitation. However, it is not enough for the development of TN. The appearance of pathological activity in the somatosensory cortex of the cerebrum and its involvement in the pathological algic system is necessary.
Clinical manifestations
The clinical picture of TN is characterized by pronounced attacks of pain - shooting, burning, painful, unbearable. It is accompanied by both local (lacrimation, rhinorrhea, salivation) and general (hyperemia, hyperhidrosis) autonomic reactions.
It is noteworthy that during an attack, despite the sharpest pain, patients do not moan, scream, or talk. TN is “silent”. The patients seem to freeze. However, at the same time, a suffering grimace appears on the face - a “pain tic”. Patients try to strongly squeeze the painful area of ​​the face with their hand “antagonist gesture”. A light touch to this area intensifies the attack or provokes it. The duration of painful paroxysm is on average 5-20 s, but not more than 2 minutes. The frequency of attacks can be very different depending on the duration of the disease and the effectiveness of treatment, up to the highest - up to several hundred times a day, completely exhausting the patient. Patients can indicate the area where the attack occurs. Clarification of this zone of origin of painful paroxysm is important for determining the affected branch of the trigeminal nerve.
An attack of pain can be provoked by various factors: talking, laughing, chewing, shaving, washing, brushing teeth, etc. In severe cases, due to pain, patients cannot eat, drink or speak, so as not to provoke an attack. This often leads to social isolation of the patient and weight loss.
An important feature of the TN is the presence of trigger, or hammer, zones. Although their localization on the face may vary from person to person, for each patient it remains constant and is well known to him. These zones can be located on the lips, wings of the nose, eyebrows, chin, and in some cases in the area of ​​the external auditory canal. Sometimes the trigger zones can move from one area of ​​the face to another. However, this is limited only to the branch of the nerve involved in the pain syndrome. A refractory period is characteristic, which consists in the inability to cause an attack within a certain period of time (from 30 to 5 minutes) when the trigger zones are irritated immediately after the end of the previous attack.
An interesting fact is that painful stimulation with a sharp needle does not cause a painful attack, while a light touch or a cold sensation does. The localization of trigger zones on the gums, tongue and palate prevents eating and speaking.
In most cases, pain paroxysm occurs against the background of apparent complete health. However, sometimes the disease can begin gradually with an unpleasant sensation of twitching, “electrification” of the face, or toothache, which serves as a reason to visit the dentist. Sometimes in the interictal period there is mild, pressing or burning pain.
Paroxysms of pain are often accompanied by symptoms of damage to the autonomic nervous system. A correlation has been established between the severity of pain and the degree of autonomic dysfunction.
K.Ya. Ogleznev et al. In patients with TN, lacrimation and dilation of the vessels of the conjunctiva of the eye were noted only when the ophthalmic branch of the trigeminal nerve was involved in the pain syndrome.
The pain syndrome is always accompanied by contraction of the muscles of the corresponding half of the face and retraction of the corner of the mouth. These muscle contractions are referred to as tonic and clonic convulsions, resulting from the transfer of excitation from the trigeminal nucleus to the facial nerve. These tic-like contractions represent an emotional-reactive response to pain and reflect a behavioral response, and not simply a switch of impulses from the trigeminal nucleus to the facial nucleus in the brain stem.
Sensitivity disorders are usually not detected, however, in some cases mild hypoesthesia or hyperpathia is detected.
The clinical picture of TN is in many ways similar to the manifestations of neuralgia of the glossopharyngeal nerve, idiopathic pain syndrome in the innervation zone of which is rare and accounts for one case in 60-100 manifestations of TN. A typical picture of neuralgia of the glossopharyngeal nerve is expressed by unilateral sharp pain in the root of the tongue, tonsils and pharynx, radiating into the external auditory canal or deep into the ear. In these cases, as with TN, paroxysms of pain are short-term and are provoked by touching the pharynx, the back of the tongue, but most often occur during swallowing. To prevent saliva from getting onto the affected part of the pharynx, patients are forced to sleep on the opposite side. Sometimes the disease can begin with unpleasant sensations in the tonsils and pharynx. With neuralgia of the glossopharyngeal nerve, sensory disorders are usually not detected. In the early stages of the disease, long-term remissions are observed, but later the pain becomes almost constant and painful. During an attack, there is a sharp opening of the mouth, flow of saliva, and sometimes a feeling of strong distension of the throat. Intense paroxysmal pain in the pharynx may be accompanied by cardiac arrest or fainting.
In the literature, there are various names for facial pain associated with damage to the intermediate nerve: atypical facial neuralgia, neuralgia of the pterygopalatine ganglion, erythromelalgia, Horton's syndrome, histamine cephalgia, neuralgia of the greater petrosal nerve, periodic migraine neuralgia. Even such an incomplete listing of the names of diseases and syndromes indicates the existing confusion in the interpretation of the problem of facial neuralgia.
E. Sachus cited 4 cases of facial and headache pain incurable by conservative methods, completely eliminated after transection of the intermediate nerve. The author draws attention to the need to find alternative pathways for pain, since in one of the cases he described, the pain disappeared only after transection of the vestibulocochlear nerve. This may be explained by the fact that several thin fascicles of the intermediate nerve may run along with the VIII cranial nerve.
J.R. Hunt described two forms of geniculate ganglion neuralgia: otological, in which pain is localized deep in the ear with irradiation into the deep structures of the face, and prosopalgic. The first form represents a syndrome of severe, often unbearable pain in the depths of the ear or in front of it. It occurs periodically, at times it is paroxysmal in nature, but more often it is constant. In this case, sometimes trigger zones are identified anterior to the ear or in the external auditory canal. The disease can occur with remissions, the duration of which decreases as the process progresses.
The prosopalgic form is manifested by attacks of rapidly increasing pain, burning or pulsating in the depths and around the eye. These pains often radiate to the temple, ear, frontal area and upper jaw. Characterized by lacrimation, vasodilatation of the conjunctiva of the eye, nasal congestion and rhinorrhea on the side of the pain syndrome. Redness of the face with a feeling of heat is often noted. In almost half of the cases of the disease, Bernard Horner syndrome occurs (ptosis, miosis, enophthalmos).
Patients experience several attacks of facial pain during the day, especially at night. Mostly men suffer - 90% of cases. The disease begins at a young age. The pain is so severe that patients moan, scream, cry (unlike those suffering from TN) and can make a suicide attempt.

Diagnostics
The criteria for diagnosing TN are:
1. Paroxysms of attacks of facial or head (frontal) localization lasting on average 5-20 s, but not more than 2 minutes.
2. Pain is characterized by at least 4 of the following symptoms:
- sharp expression, cruelty;
- occurs mainly when exposed to trigger points or when performing a number of everyday activities: eating, talking, washing your face, shaving, brushing your teeth;
- during an attack, “pain behavior” is observed (patients try not to move, freeze, do not speak);
- in the interictal period there are no neurological symptoms.
3. Each patient's attacks are stereotypical, but individual.
4. The diagnosis is established by excluding other causes of facial pain by clarifying anamnestic data, a thorough neurological examination, and, if necessary, using additional special research methods, incl. computer and magnetic resonance imaging, electrophysiological, ultrasound, biochemical and others.

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Trigeminal neuralgia– this is one of the most common diseases of the peripheral nervous system, the main clinical symptom of which is intense pain of a paroxysmal nature, noted in the innervated areas of the face. For timely and effective treatment of pathogenic processes, you need to have an understanding of the types of neuralgia, the etiology of their development, the main symptoms, as well as modern methods of diagnosis and therapy.

What is trigeminal neuralgia?

The trigeminal nerve begins in the anterior zone of the Varoliev bridge, which is located near the cerebellar peduncles. It includes 2 types of roots: large sensory and small motor. These structures are directed to the tops of the temporal bones.

The fibers of the motor roots, in combination with the third sensitive branch, exit through the foramen ovale, and then connect with it. In the cavity of the cavity near the pyramidal bones there are structures of the semilunar ganglion. The trisensory branches of the trigeminal nerve emerge from them.

Trigeminal neuralgia is a pathological condition in which pain is noted along the nerve fibers. The structures of the trigeminal nerve take part in the innervation of the orbital zone, lips, cheeks, gums, jaws and nose.

Along the course of the nerve to the areas of innervation, the branches pass through various anatomical structures, in which they can be subject to irritation and compression. In most cases, the jaw branches are affected. Neuralgia of the first branch is extremely rare.

Helpful information

When the trigeminal nerve is damaged, various disorders can develop. Most often, there is a sharp increase or decrease in the sensitivity of the innervated zones. In some situations, part of the face becomes numb, and there are also disorders in the mobility of the facial muscles.

Types of neuralgia

All types of trigeminal neuralgia are divided into 2 types:

1. Primary neuralgia. It is a separate disease and develops as a result of compression of nerve fibers or poor circulation in the affected area.
2. Secondary neuralgia. Its development is due to the presence of concomitant diseases. Among them, the most common are benign and malignant neoplasms, as well as severe infectious lesions of the body.

Causes

Among the factors leading to the formation of pathological processes in nerve fibers, the most common are:

1. Compression of nerve structures where they exit the skull. Most often, the causes of this are traumatic lesions of the temporal bone, jaw, post-traumatic scars, congenital anomalies of bone tissue development, benign and malignant neoplasms, vascular pathologies, cerebral strokes, arterial hypertension, osteochondrosis of the spinal column, acute infectious diseases, sclerotic damage to the myelin sheaths.
2. Diseases of the nervous system. These include cerebral palsy, inflammation of the meninges of bacterial and viral etiology, multiple sclerosis, epilepsy, cancer and encephalopathy, which develop as a result of head injuries, hypoxia, infectious lesions and metabolic disorders.
3. Odontogenic factors. Among them are dental fluxes, jaw injuries, the consequences of filling and tooth extraction, as well as other surgical procedures performed in the facial area.
4. Exposure to viral agents. Poliomyelitis, herpes viruses, and HIV can lead to trigeminal neuralgia.

Nature of pain and main symptoms

Clinical manifestations of trigeminal neuralgia are divided into several groups - pain syndrome, reflex and motor disorders, as well as vegetative-trophic disorders. The pain is intense, with a sharp, paroxysmal character. The duration of spasms ranges from a few seconds to 4-5 minutes. They may have the following localization:

1. Ophthalmic branch - forehead, bridge of the nose, upper eyelid, inner corner of the eye, scalp, ethmoid sinus.
2. Maxillary branch – upper jaw and lip, teeth, cheeks, maxillary sinus, lower eyelid, nasal mucous membranes.
3. Mandibular branch - the lower part of the cheek, lips and neck, teeth, back of the head, chin and anterior surface of the lower jaw.

Reflex and motor disorders in most cases are manifested by muscle spasms. During attacks, the muscle fibers of the orbicularis oculi muscles involuntarily contract, which provokes the development of blepharospasm. These processes can spread to the chewing muscles, and in advanced cases - to the entire half of the face.

Vegetative-trophic disorders are observed during attacks, and in the early stages of the development of pathological processes they are weakly expressed. Over time, they become more noticeable and are manifested by the following symptoms:

• lacrimation, drooling, runny nose;
• hyperemia of the skin;
• dry or greasy skin;
• swelling of the face;
• eyelash loss.

In the absence of timely treatment, the formation of points of painful pathological activity occurs in the structures of the thalamus. As a result, the nature and location of pain changes. This stage is characterized by the following signs:

• spread of pain to the entire face;
• hyperesthesia of the skin;
• development of pain from paroxysmal to chronic;
• increased vegetative-trophic disorders.

In most cases, trigeminal neuralgia is diagnosed in people aged 35-45 years. The right half of the face is most often affected. In 5-7% of cases the disease is bilateral. Exacerbation of pathological processes is typical in the autumn-spring season.

Diagnostics

To diagnose the disease, you need to consult a neurologist. The diagnosis is made based on the patient’s complaints, medical history, and the results of objective and neurological examinations. The main diagnostic criterion is the presence of trigger points that correspond to the course of the nerve branches. In order to clarify the etiology of pathological processes, the doctor may prescribe instrumental examination methods:

1. Magnetic resonance angiography. It is used to detect compression lesions of blood vessels. The information content of the technique is high in the presence of large vascular loops or aneurysms.
2. Computed tomography of the skull. With its help, the skull is examined for changes in the size and location of bone structures. It makes it possible to detect narrowing of the canals and foramina, which are the gates for the branches of the trigeminal nerve.
3. Magnetic resonance imaging of the brain. This technique is used to exclude the presence of space-occupying formations as a cause of compression of nerve fibers.

Trigeminal neuralgia must be differentiated from prosopalgia of myogenic, vascular and psychogenic etiology. The presence of autonomic disorders indicates the vascular nature of paroxysms. Psychogenic facial pain is distinguished by its paroxysmal nature and varied pattern of pain sensations. In order to exclude rhinogenic, ophthalmic and odontogenic factors, consultations with an otolaryngologist, ophthalmologist and dentist are necessary.

Treatment methods

Treatment of trigeminal neuralgia is carried out comprehensively. For this purpose, the following techniques are used:

• drug therapy;
• surgical interventions;
• physiotherapy;
• facial gymnastics;
• alternative medicine recipes.

Drug treatment

The choice of medications, dosages and duration of the course of their use for trigeminal neuralgia is carried out by a neurologist. The main groups of drugs for treating the disease are:

• antispasmodics and muscle relaxants;
• anticonvulsants;
• non-steroidal anti-inflammatory drugs;
• painkillers;
• vitamin complexes.

Antispasmodics and muscle relaxants are used to treat neuralgia associated with multiple sclerosis. They relax muscles and eliminate pain. The most effective representatives of these groups are Sirdalud and Mydocalm.

Sirdalud is effectively used for various forms of trigeminal neuralgia. Side effects of the drug include sleep disturbances, weakness, fatigue, constant drowsiness, dizziness, dry mouth, and decreased blood pressure. The daily dose of the drug is 12-24 mg. It is divided into 2-4 doses with breaks at equal intervals.

Mydocalm has a similar medicinal effect to Sirdalud. The drug is taken 3 times a day, every 8 hours. If the wrong dosage is prescribed, headaches, decreased blood pressure, and a feeling of muscle weakness may develop. If you are intolerant to the active ingredients of the product, itching, urticaria, nausea and vomiting occur.

The main anticonvulsant drug in the treatment of trigeminal neuralgia is Phenlipsin. The main active component of the drug is carbamazepine. Taking the drug allows you to get rid of pain, possible cramps and paroxysms of muscle fibers. The dosage is calculated based on the availability of data on the patient’s weight, age and possible concomitant diseases.

The use of the drug in large doses is recommended until pain is completely eliminated with further maintenance therapy. The most common side effects of treatment with Phenlipsin are nausea, vomiting, increased drowsiness, gastrointestinal disorders, and muscle ataxia.

If there is no effect of treatment with the drug, the neurologist may prescribe other medications that have a similar effect. These include Lamotrigine, Baclofen, Gabapentin and Prebalgin.

Baclofen and Lamotrigine are the drugs of choice in patients with multiple sclerosis. Side effects of these drugs include gastralgic disorders, hypotension, drowsiness, dizziness and withdrawal syndrome.

Nonsteroidal anti-inflammatory drugs are used to eliminate inflammatory processes that have led to compression of the trigeminal nerve fibers. Among them, Ibuprofen, Nimesulide, and Indomethacin are most often used. They have no absolute contraindications and also have a low likelihood of developing side effects.

In order to relieve acute pain in the jaws, back of the head and ears, painkillers are prescribed. In this case, Dexalgin, Baralgin, and Paracetamol have the most pronounced therapeutic effect. They are recommended to be taken after meals. This will reduce the effect of the active components on the gastric mucosa. The use of drugs in this group is contraindicated in the presence of bronchial asthma, chronic bleeding, gastritis, stomach and duodenal ulcers, as well as liver diseases.

B vitamins are prescribed in the form of tablets or injection ampoules. As primary therapy, it is recommended to use drugs in the form of a course of injections, and for maintenance treatment - in the form of dragees or tablets. Electrophoresis with vitamins is also possible.

This group of drugs is prescribed in combination with other medications. Vitamins can reduce the severity of pain, promote the restoration of damaged nerve fibers, and also increase the effectiveness of low-dose medications used. This makes it possible to reduce the negative impact on the patient’s body.

The most effective preparations of B vitamins include Neurobion, Milgamma, Neuromultivit and Combilipen. If taken, it is possible to develop allergic skin reactions, arrhythmias and increased sweating.

The following groups can be used as auxiliary medications:

1. Vascular agents. They help improve microcirculation, as well as increase metabolic activity and rapid regeneration of affected nerve fibers. The most effective medications for the treatment of trigeminal neuralgia are Actovegin and Pentoxifylline.
2. Antibacterial and antiviral agents. Their action is aimed at combating pathogenic microorganisms that have led to the development of pathological processes in nerve structures. These include Cefotaxime, Cefuroxime, Ceftriaxone, Cycloferon, Acyclovir, Oseltamivir.
3. Corticosteroids. With their help, normalization of microcirculation and elimination of edema in areas of inflammation is achieved. Among this group, Dexamethasone and Prednisolone are used to treat trigeminal neuralgia.

During the recovery period, it is possible to prescribe Neuromidin. It improves the quality of nerve impulses and promotes the regeneration of affected fibers of the trigeminal nerve.

Surgical intervention

If conservative treatment of the disease fails, doctors prescribe surgical interventions. For this, the following types of manipulations are used:

• decompression of nerve structures;
• radiofrequency destruction of affected fibers;
• percutaneous removal of the inflamed nerve.

Physiotherapy

Physiotherapeutic procedures reduce the severity of pain and also accelerate the regeneration processes of affected structures. The main methods of physiotherapy for trigeminal neuralgia are:

• electrophoresis;
• ultra-high frequency treatment;
• laser therapy;
• ultraviolet irradiation;
• magnetic therapy;
• electric currents.

Using a set of exercises for trigeminal neuralgia can alleviate the severity of pain attacks and reduce compression of the branches of the trigeminal nerve. In addition, among the positive effects of exercise therapy are:

• improvement of microcirculation;
• increased conductivity of nerve impulses;
• preventing the development of muscle congestion.

You need to perform the exercises in front of a mirror. This will allow you to control the process. The facial gymnastics complex includes:

• turns and tilts of the head;
• bringing your lips together into a tube and stretching them into a wide smile;
• cheek retraction;
• drawing air into the cheeks and then exhaling through a narrow gap in the lips;
• closing and opening the eyes;
• raising and lowering eyebrows.

Folk remedies

The use of alternative medicine is recommended only after consultation with your doctor. When treating trigeminal neuralgia, the most effective recipes are:

1. Compresses with boiled beets and black radish juice. To do this, you need to boil the beets, grate them thoroughly on a coarse grater and pour black radish juice over the mixture. You can also add lavender tincture and essential oil. The resulting mixture is placed in a bandage envelope and placed in the ear canal on the side of inflammation or tied to the area where pain is most often noted. Compresses are applied at night every day for a week. After this you need to take a break for 1-1.5 months.
2. Tea with honey and chamomile. After preparing the product, you need to take it into your mouth in small sips and hold it for 2-3 minutes. This will reduce the severity of the clinical picture of the pathology when the maxillary or mandibular branches of the nerve are affected.
3. Lotions with horseradish root. One root of the plant is grated on a coarse grater, after which the resulting mass is wrapped in a small piece of cloth or napkin and applied to the site of inflammation.

Forecast

Timely contact with specialists ensures complete recovery in 75% of cases. In the absence of adequate therapy, trigeminal neuralgia becomes chronic, which significantly complicates treatment.

Helpful information

An unfavorable course of the disease is observed in insulin-dependent diabetes mellitus and arterial hypertension. Also, a disappointing prognosis is observed with deep damage to nerve branches in elderly people.

Trigeminal neuralgia has virtually no effect on the general condition of the human body. However, in advanced cases, paresis and paralysis of certain muscle groups may develop, which affects a number of social and psychological aspects of the patient’s life.

Prevention

Specific prevention of the disease has not been developed. Among nonspecific measures to prevent the development of the disease, the most effective are:

• timely treatment of concomitant diseases that increase the risk of trigeminal neuralgia;
• controlling the course of existing chronic pathologies;
• avoiding hypothermia and stress;
• regular hardening and increasing the body's immune defense;
• maintaining an active lifestyle, spending free time in the fresh air;
• attending routine medical examinations.

If you detect any symptoms of trigeminal neuralgia, it is recommended to immediately consult a neurologist. Timely detection of pathology reduces the likelihood of complications and allows you to prescribe the most effective treatment tactics. This makes it possible to completely restore the function of the affected nerve and improve the patient’s quality of life.

Trigeminal neuralgia is a pathology in which there is damage to the peripheral nerve endings located in the facial area. It is usually caused by inflammation of one or more branches of the trigeminal nerve.

The symptoms and treatment of facial neuralgia are described in this article. If you are suffering from this disease, contact the CELT Pain Clinic. Despite the fact that this pathology is difficult to treat, our specialists have everything necessary to make it successful.

Causes of trigeminal neuralgia

Symptoms of facial neuralgia occur due to compression of the trigeminal nerve root by the cerebellar artery at its entrance to the brain stem. Destruction of the nerve fiber sheath occurs due to the fact that the artery either compresses the nerve or wraps around it. This pathology occurs due to inflammatory processes in the nasal mucosa, periodontal tissue or other organs, which lead to a narrowing of the lumen of the canal through which the nerve passes.

In addition, trigeminal neuralgia can develop due to:

• hypothermia of nerve fibers with subsequent spasms of facial muscles;
• disruptions in the functioning of the endocrine system;
• compression due to growth of tumors;
• pathologies of neurogenic and vascular nature;
• herpes virus.

Clinical manifestations of neuralgia

The following symptoms are characteristic of trigeminal neuralgia:

• attacks of severe pain;
• increased pain during any actions with the mouth (chewing, opening, etc.);
• facial distortion;
• concentration of pain in the eyes, ears, teeth, mouth;

Trigeminal facial neuralgia is characterized by attacks of stabbing, cutting, pulling pain lasting up to 1 minute. In the vast majority of cases, one side of the face is affected, but there are cases when pathological processes spread to the entire face. Painful sensations can be projected into the teeth and can cause the removal of a completely healthy tooth.

Diagnosis of neuralgia

Diagnosis of neuralgia in the CELT Clinic does not cause difficulties, since it has a number of pronounced signs. When talking about the clinical manifestations of the disease, patients try not to touch the affected side of the face and remain in a tense state because they expect a new attack.

Studies are carried out on the functions of the facial and trigeminal nerves, which begin with assessing the symmetry of the patient’s face. In addition, a number of tests are carried out to check taste and sensitivity.

For the most accurate diagnosis of pathological processes in the nerves of the face, an ultrasound scan of the nerves is performed.

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Treatment of neuralgia

Treatment of neuralgia is a long and difficult process, but doctors at the CELT Pain Clinic know how to carry it out with maximum positive effect. For this purpose it is used for the treatment method.

Conservative method

Conservative treatment involves taking medications:

• antispasmodics;
• anticonvulsants

• Bernard currents;
• acupuncture;
• paraffin applications.

If this treatment method does not bring the desired effect, the attending physician may decide on surgical treatment.

Surgical method

• microvascular decompression of the root using implants that prevent compression on the nerve;
• radiofrequency destruction, which involves destruction of the nerve root;

The most modern method is radiofrequency ablation of the Gasserian ganglion, which involves minimal surgical intervention and is most effective. Just one procedure allows you to get rid of pain.

Contact the CELT Pain Clinic and live without pain!